Cirrhosis Caused by Chronic Hepatitis C

Cirrhosis Caused by Chronic Hepatitis C

Liver cirrhosis (LC) is a critical stage of chronic liver disease, including that caused by hepatitis C virus (HCV). In the absence of antiviral therapy, 67%-91% of patients with HCV-related LC patients die of liver-related causes, including hepatocellular carcinoma (HCC) and liver failure. Among the therapeutic strategies used to prevent liver-related complications in these patients is standard therapy with pegylated interferon and ribavirin, which induces a sustained virological response (SVR) in 25% of HCV genotype 1-infected patients and in 69% of patients infected with genotypes 2 and 3. SVR in patients with HCV-related LC has been associated with reduced rates of hepatic decompensation, HCC, and mortality. More recently developed direct-acting antiviral agents have shown excellent antiviral efficacy, with preliminary data demonstrating that an interferon-free regimen that includes these direct-acting antiviral agents achieved SVR in more than 50% of patients with HCV genotype 1 LC. Branched-chain amino acid supplementation, improvement of insulin resistance, and the use of β-blockers for portal hypertension may also reduce liver-related complications. Here, we review advances in antiviral and adjunctive therapies for improved outcomes in patients with HCV-associated LC.

Core tip: Liver cirrhosis (LC) is the critical stage of hepatitis C virus (HCV)-related chronic liver disease. Many studies of HCV-related LC patients have indicated that sustained virological response (SVR) after interferon therapy is highly associated with reductions in hepatic decompensation, hepatocellular carcinoma incidence, and mortality. Furthermore, direct-acting antiviral agents have shown excellent antiviral efficacy. Preliminary data have indicated that an interferon-free regimen achieved SVR for more than 50% of patients with LC due to HCV genotype 1. Branched-chain amino acid supplementation, improvement of insulin resistance, and the use of β-blockers for portal hypertension may also contribute to a reduction in liver-related complications.

Hepatitis C virus (HCV) infection is one of the most serious global health problems. The incidence of HCV infection is increasing, with over 185 million people infected worldwide. Moreover, approximately 370000 HCV-infected individuals die of liver-related causes each year. HCV-related liver disease can progress in an insidious manner over several decades. The advanced forms of the disease are liver cirrhosis (LC) and hepatocellular carcinoma (HCC). Approximately 20%-30% of subjects chronically infected with HCV are estimated to develop LC 15-25 years later. A recent systematic review found that, in HCV-infected patients with compensated LC, 2.8%-11.7% develop hepatic decompensation, 1.8%-8.3% develop HCC, and 2.7%-6.7% die or undergo liver transplantation each year. In the absence of antiviral therapy, 67%-91% of patients with HCV-related LC die due to liver-related causes, including HCC or hepatic failure. Hence, LC is a critical stage in HCV-related chronic liver disease, as is LC due to other causes, including hepatitis B virus (HBV), alcohol abuse, and nonalcoholic steatohepatitis. Here, we review advances in therapeutic strategies to prevent hepatic decompensation, hepatocarcinogenesis, and mortality in patients with HCV-related LC.